English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background Obesity is associated with a state of low-grade chronic inflammation, commonly causing insulin resistance (IR) and type 2 diabetes mellitus (T2D). The NLRP3 inflamassome is a key mediator of metabolic inflammation, and it has been shown to be activated in macrophages of newly diagnosed insulin resistant-T2D patients. In humans, reduction in NLRP3 expression in adipose tissue is linked to decreased inflammation and improved insulin sensitivity in obese T2D patients. Recently, it was demonstrated that the lipolytic factor CGI-58 is an endogenous suppressor of NLRP3 activity in animal models. Therefore, the aim of this study was to evaluate CGI-58 and NLRP3 gene expressions in adipose tissue from individuals with different obesity degrees and their association with metabolic variables.

Evaluation of NLRP3 inflamassome expression and its endogen inhibitor CGI-58 in subjects with different obesity degrees